Vascular endothelial growth factor and heparin in a biologic glue promotes human aortic endothelial cell proliferation with aortic smooth muscle cell inhibition

Sealing of Polyester Prostheses with Autologous Fibrin Glue and Bone Marrow

“…Further study will be necessary to develop biointeractive matrixes that modulate the healing process by selective promotion of endothelial cell proliferation and inhibition of smooth muscle cell production. Pathways for this research include matrixes containing growth factors and heparin in various proportions 15,[33][34][35] or antisense factors that act selectively against growth factors stimulating extracellular matrix production. [36][37][38] In conclusion, sealing of vascular prosthetic grafts with an autologous matrix composed of fibrin glue and bone marrow cells is clinically feasible.…”

Activation Transcription Factor-4 Induced by Fibroblast Growth Factor-2 Regulates Vascular Endothelial Growth Factor-A Transcription in Vascular Smooth Muscle Cells and Mediates Intimal Thickening in Rat Arteries Following Balloon Injury

“…We did not observe any significant mitogenic effect of VEGF-A (unlike FGF-2) on SMC growth after 3 days ( Figure 8E, top), consistent with previous reports. 28 ATF-4 overexpression, on the other hand, stimulated SMC proliferation after 3 days, and this growth was unaffected by the presence of neutralizing VEGF-A antibodies ( Figure 8E, bottom). These data demonstrate that the mitogenic effect of ATF-4 on SMCs is mediated by factors other than VEGF-A.…”

“…This study provides the first demonstration of ATF-4 induction in vascular SMCs by arterial balloon injury in vivo and mechanical injury in vitro. It is also the first demonstra- ) from the human VEGF-A gene containing an ATF-4 recognition element, also called an amino acid response element, 28 sequences were cloned into pGL3-prom vector, and 5 g was transfected into rat SMCs, together with internal control plasmid pRL-TK. Luciferase activity was determined in the cell lysates after 24 hours.…”

“…49 On one hand, some reports indicate that VEGF-A is an endothelial cell mitogen with poor, if any, positive influence on SMC proliferation. 28 VEGF-A is thought to attenuate SMC hyperplasia by stimulating reendothelialization. 50,51 On the other hand, several lines of evidence indicate that VEGF-A stimulates neointima formation.…”

Vascular tissue engineering by computer-aided laser micromachining

“…Heilbrunn & Wilson (1949), have suggested that heparin directly acts on smooth muscle cells. More recent work by Weatherford et al (1996) demonstrated by means of in vitro assays that heparin and vascular endothelial growth factor together inhibited proliferation of human aortic smooth muscle cells as well as stimulated proliferation of human aortic endothelial cells; fibrin glue or another biological glue containing both biological molecules may improve patency of vascular grafts by selectively promoting endothelial cell proliferation while inhibiting smooth muscle cell proliferation. Vascular endothelial growth factor and heparin were selected to develop differential adherent interfaces for growth of HAAE-1 human aortic endothelial cells and HA-VSMC human aortic smooth muscle cells.…”